Evidence map›Paper›PMID 31211500›Full record

ArticleJournal of cellular and molecular medicine2019

Knockdown of KDM1A suppresses tumour migration and invasion by epigenetically regulating the TIMP1/MMP9 pathway in papillary thyroid cancer.

WenQian Zhang, Wei Sun, Yuan Qin, CangHao Wu, Liang He, Ting Zhang, Liang Shao, Hao Zhang, Ping Zhang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. The Changing Face ofFrontiers in surgery · 2020
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

WenQian ZhangDepartment of Thyroid Surgery, The First Hospital of China Medical University, Shenyang Liaoning Province, China.
Wei SunDepartment of Thyroid Surgery, The First Hospital of China Medical University, Shenyang Liaoning Province, China.
Yuan QinDepartment of Thyroid Surgery, The First Hospital of China Medical University, Shenyang Liaoning Province, China.
CangHao WuDepartment of Thyroid Surgery, The First Hospital of China Medical University, Shenyang Liaoning Province, China.
Liang HeDepartment of Thyroid Surgery, The First Hospital of China Medical University, Shenyang Liaoning Province, China.
Ting ZhangDepartment of Thyroid Surgery, The First Hospital of China Medical University, Shenyang Liaoning Province, China.
Liang ShaoDepartment of Thyroid Surgery, The First Hospital of China Medical University, Shenyang Liaoning Province, China.
Hao ZhangDepartment of Thyroid Surgery, The First Hospital of China Medical University, Shenyang Liaoning Province, China.ORCID 0000-0002-9938-8433
Ping ZhangDepartment of Thyroid Surgery, The First Hospital of China Medical University, Shenyang Liaoning Province, China.
First Hospital of China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epigenetic dysregulation plays an important role in cancer. Histone demethylation is a well-known mechanism of epigenetic regulation that promotes or inhibits tumourigenesis in various malignant tumours. However, the pathogenic role of histone demethylation modifiers in papillary thyroid cancer (PTC), which has a high incidence of early lymphatic metastasis, is largely unknown. Here, we detected the expression of common histone demethylation modifiers and found that the histone H3 lysine 4 (H3K4) and H3 lysine 9 (H3K9) demethylase KDM1A (or lysine demethylase 1A) is frequently overexpressed in PTC tissues and cell lines. High KDM1A expression correlated positively with age <55 years and lymph node metastasis in patients with PTC. Moreover, KDM1A was required for PTC cell migration and invasion. KDM1A knockdown inhibited the migration and invasive abilities of PTC cells both in vitro and in vivo. We also identified tissue inhibitor of metalloproteinase 1 (TIMP1) as a key KDM1A target gene. KDM1A activated matrix metalloproteinase 9 (MMP9) through epigenetic repression of TIMP1 expression by demethylating H3K4me2 at the TIMP1 promoter region. Rescue experiments clarified these findings. Altogether, we have uncovered a new mechanism of KDM1A repression of TIMP1 in PTC and suggest that KDM1A may be a promising therapeutic target in PTC.

Indexed as

AnimalsCell Line, TumorCell MovementChromatin ImmunoprecipitationDemethylationEpigenesis, GeneticFemaleGene Expression Regulation, NeoplasticHistone DemethylasesHistonesHumansLymphatic MetastasisMaleMatrix Metalloproteinase 9MiceMice, NudeHistone DemethylasesHistonesKDM1A protein, humanMatrix Metalloproteinase 9MMP9 protein, humanTIMP1 protein, humanTissue Inhibitor of Metalloproteinase-1H3K4me2KDM1Alymphatic metastasisthyroid cancerTIMP1

Identifiers

PMID31211500
PMCPMC6653290
OpenAlexW2949161518

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.